dc.contributor.author | Gasa Colom, Laura | |
dc.contributor.author | Sánchez Botet, Abril | |
dc.contributor.author | Quandt Herrera, Eva | |
dc.contributor.author | Hernández Ortega, Sara | |
dc.contributor.author | Jiménez Jiménez, Javier | |
dc.contributor.author | Carrasco García, Miguel Ángel | |
dc.contributor.author | Simonetti, Sara | |
dc.contributor.author | Kron, Stephen J. | |
dc.contributor.author | P.C. Ribeiro, Mariana | |
dc.contributor.author | Nadal, E | |
dc.contributor.author | Villanueva, Alberto | |
dc.contributor.author | Clotet Erra, Josep | |
dc.date.accessioned | 2019-10-13T18:03:43Z | |
dc.date.available | 2019-10-13T18:03:43Z | |
dc.date.issued | 2017-08-31 | |
dc.identifier.citation | Gasa, L., Sanchez-Botet, A., Quandt, E., Hernández-Ortega, S., Jiménez, J., Carrasco-García, M. A. & Villanueva, A. (2017). «A systematic analysis of orphan cyclins reveals CNTD2 as a new oncogenic driver in lung cancer». Scientific reports, 7(1), 10228. | ca |
dc.identifier.issn | 2045-2322 | ca |
dc.identifier.uri | http://hdl.handle.net/20.500.12328/1257 | |
dc.description.abstract | As lung cancer has increased to the most common cause of cancer death worldwide, prognostic
biomarkers and efective targeted treatments remain lacking despite advances based on patients’
stratifcation. Multiple core cyclins, best known as drivers of cell proliferation, are commonly
deregulated in lung cancer where they may serve as oncogenes. The recent expansion of the cyclin
family raises the question whether new members might play oncogenic roles as well. Here, we
investigated the protein levels of eight atypical cyclins in lung cancer cell lines and formalin-fxed and
parafn-embedded (FFPE) human tumors, as well as their functional role in lung cancer cells. Of the new
cyclins evaluated, CNTD2 was signifcantly overexpressed in lung cancer compared to adjacent normal
tissue, and exhibited a predominant nuclear location. CNTD2 overexpression increased lung cancer
cell viability, Ki-67 intensity and clonogenicity and promoted lung cancer cell migration. Accordingly,
CNTD2 enhanced tumor growth in vivo on A549 xenograft models. Finally, the analysis of gene
expression data revealed a high correlation between elevated levels of CNTD2 and decreased overall
survival in lung cancer patients. Our results reveal CNTD2 as a new oncogenic driver in lung cancer,
suggesting value as a prognostic biomarker and therapeutic target in this disease. | en |
dc.format.extent | 12 | ca |
dc.language.iso | eng | ca |
dc.publisher | Scientific Reports | ca |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 International | * |
dc.rights | This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. | |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject.other | Lung cancer | en |
dc.subject.other | Cáncer de pulmón | es |
dc.subject.other | Càncer de pulmó | ca |
dc.subject.other | CNTD2 | ca |
dc.subject.other | Cyclins | en |
dc.subject.other | Ciclines | ca |
dc.subject.other | Ciclinas | es |
dc.title | A systematic analysis of orphan cyclins reveals CNTD2 as a new oncogenic driver in lung cancer | en |
dc.type | info:eu-repo/semantics/article | ca |
dc.description.version | info:eu-repo/semantics/acceptedVersion | ca |
dc.embargo.terms | cap | ca |
dc.subject.udc | 616.2 | ca |
dc.identifier.doi | https://dx.doi.org/10.1038/s41598-017-10770-8 | |